In 1854, Max Durand-Fardel (1816-1899), a keen observer of the peculiar lesions affecting the brains of the elderly, described interstitial brain atrophy, a condition characterized by loss of tissue density in the white matter.1,2 However, Durand-Fardel found “no symptom characteristic of this change.” 2 Forty years later, Otto Binswanger (1852-1929), separated from neurosyphilis a vascular form of dementia characterized pathologically by extensive periventricular white matter lesions (WML) with typical preservation of subcortical arcuate fibers.3,4 Since then, the role played by WML in the elderly has evolved from a purely casual marker of aging to an important cause of disability, depression, and vascular dementia.4 In this issue of the ARCHIVES, Prins et al5 analyze the impact of WML on incident dementia in the prospective population-based Rotterdam Scan Study. For the purpose of their analyses, the authors divided WML topographically into periventricular and subcortical. After a mean follow-up of 5.2 years, dementia developed in subjects who, at baseline, had more severe WML in all locations; however, those with increasing severity of periventricular WML had a higher risk of developing dementia independently of other risk factors (hazard ratio, 1.67; 95% confidence interval, 1.25-2.24; per standard deviation rise in periventricular WML severity). The association between subcortical WML and dementia was less prominent. Therefore, the results of this large, methodologically flawless population-based study confirm the association between extensive WML and the risk of dementia.